It is increasingly apparent that exercise training brings about significant physiological and biochemical alterations in mammalian systems. Many of these alterations have certain health implications as seen in the prevention of and rehabilitation from coronary heart disease. Cardiovascular adaptations, that significantly reduce cardiac work and provide for a more effective circulation, are probably subsequent to fundamental changes within the working muscles. This includes a nearly 2-fold increase in the capacity to produce ATP via oxidative metabolism. We have recently shown that changes in the degradation and synthesis rates are responsible for this adaptation. This indicates that cellular processes concerned with mitochondrial synthesis and degradation are changed with endurance training. Studies outlined in this proposal would further clarify the changes in cellular processes which result in the development and maintenance of this increased oxidative capacity. Interest is especially focused on the response of the three different skeletal muscle fiber types, since considerable differences exist in the metabolic and physiologic function of these fibers. Studies evaluating lysosome involvement in the degradation of mitochondria are included. Turnover rates of different mitochondrial components that are synthesized by the ribosomal and mitochondrial synthetic systems will be identified. These data should describe a coordinated scheme of mitochondrial synthesis and degradation. One notable effect of endurance training is an increased work capacity. Investigations with muscle stimulated in vitro will be undertaken to explore the physiological significance of the biochemical changes induced by endurance training in the absence of cardiovascular complications. In general, these studies are designed to evaluate adaptations in skeletal muscle that appear to be fundamental to the health related benefits associated with exercise.